Ask about this productRelated genes to: LENG4 antibody
- Gene:
- MBOAT7 NIH gene
- Name:
- membrane bound O-acyltransferase domain containing 7
- Previous symbol:
- LENG4
- Synonyms:
- BB1, hMBOA-7, LPLAT
- Chromosome:
- 19q13.42
- Locus Type:
- gene with protein product
- Date approved:
- 2004-01-28
- Date modifiied:
- 2018-03-06
Related products to: LENG4 antibody
Related articles to: LENG4 antibody
- Cold waves exacerbated by global warming and the resultant sharp drops in coastal water temperature pose serious threats to the sustainability of bivalve aquaculture. The fatty acid desaturase (Fad) and membrane-bound O-acyltransferase (Mboat) gene families play essential roles in maintaining membrane lipid homeostasis and facilitating cold adaptation. Although Fad genes have been investigated in several bivalves, the role of Mboat genes in cold stress and how these two families coordinately regulate lipid remodeling under cold stress remain largely unclear. This study performed a comprehensive genome-wide identification of Fad and Mboat genes across 35 bivalve species, identifying 3-11 Fad and 6-11 Mboat members per species, classified into four (Fads, Fads6, Degs, Scd) and six (Lpcat, Mboat7, Porcn, Hhat, Dgat, Soat) subfamilies, respectively. Phylogenetic analysis revealed a significant expansion of the Fads subfamily in Mytilus and Venerida, lineage-specific expansion of Scd in Ostreida, and expansion of the Lpcat subfamily in Pectinida, Adapedonta, and Cardiida, suggesting adaptive evolution of lipid metabolic pathways in bivalves. Focusing on the noble scallop Chlamys nobilis, tissue-specific expression profiles were characterized, with CnScd1 highly enriched in blood and kidney and CnScd2 almost exclusively expressed in the female gonad. To investigate the response of these genes to cold stress, C. nobilis were exposed to acute and chronic cold stress. The results revealed complex transcriptional response patterns of the Fad and Mboat families to cold stress in bivalves, and identified multiple candidate genes showing consistent responses under both acute and chronic stress regimes, including CnScd1, which was significantly upregulated by 20-fold under both conditions, as well as CnDegs1 and CnLpcat1/2/3, which were steadily induced during chronic cold exposure. Furthermore, several CnMboat genes exhibited an inverted U-shaped expression peak around 10 °C, suggesting that this temperature may represent a critical physiological acclimation window. These results suggest that the Fad and Mboat families may be involved in membrane lipid adaptation, although the underlying mechanisms and functional outcomes still require further validation. This study provides new insights into the molecular mechanisms of cold adaptation in marine bivalves, and the above genes may serve as candidate markers for cold tolerance breeding, although further functional validation and population genetic assessments are still needed. Meanwhile, these findings also provide a theoretical foundation for molecular marker-assisted breeding of cold-tolerant varieties and the sustainable development of bivalve aquaculture. - Source: PubMed
Publication date: 2026/09/09
Su HailongZhang TaoLiu ShitongZhao NaiqianLin QingLiao WeiminZhang HongkuanZheng Huaiping - Metabolic dysfunction-associated fatty liver disease (MAFLD) usually progresses slowly, but some patients experience exceptionally rapid deterioration. We report a 38-year-old woman who progressed from biopsy-confirmed steatosis to decompensated cirrhosis within 11 months and developed recurrent graft steatosis 8 months after liver transplantation. Genetic testing revealed heterozygous variants in PNPLA3, TM6SF2, MBOAT7, and GCKR, indicating a polygenic predisposition to lipid accumulation, inflammation, and fibrogenesis. Histology and imaging analyses showed progressive steatosis with bridging fibrosis before transplantation and severe recurrence within the graft after transplantation, highlighting that transplantation does not eliminate the underlying metabolic-genetic vulnerability. This case suggests that a polygenic background may contribute to ultra-rapid disease trajectories and supports integrating genetic profiling into diagnostic and prognostic evaluation for MAFLD. Awareness of such risk patterns may guide early surveillance and long-term metabolic management even after transplantation. - Source: PubMed
Publication date: 2026/09/18
Mai Zi-LingChang BingLi Yi-LingWei HongMa Bo-Tong - Metabolic dysfunction-associated steatohepatitis (MASH) represents a major global health burden, bridging isolated steatosis, progressive fibrosis and hepatocellular carcinoma. Recent paradigms highlight ferroptosis, an iron-dependent, lipid-peroxidation-driven form of regulated cell death, as a primary lytic initiating event in metabolic liver injury. In this review, we delineate the ferroptosis-immune axis in MASH, characterising it as a self-amplifying, bidirectional circuit. In this framework, parenchymal ferroptotic rupture and damage-associated molecular pattern emission drive myeloid activation and pro-inflammatory cytokine release. This inflammatory microenvironment reciprocally triggers cell-autonomous Kupffer cell ferroptosis and homeostatic collapse. We establish a novel cell-type-specific transcriptomic framework governed by a core four-gene signature (, , and ) that maps the transition from early metabolic stress to advanced structural remodelling. Furthermore, we decode the substrate paradox of polyunsaturated fatty acids, illustrating how their role shifts from physiological signalling to executioner substrates when antioxidant systems collapse. This biophysical vulnerability is heavily primed by inherited gene polymorphisms, including , and By evaluating the sexual dimorphism embedded within these pathways, specifically how the DTL-PROX1 axis dictates distinct iron accumulation rates and lipid peroxidation sensitivities, we propose precise clinical stratification strategies. Finally, we outline actionable translational avenues, highlighting how targeting the ferroptosis-immune axis offers a highly specific therapeutic window to arrest lipotoxicity, suppress inflammation and disrupt oncogenic priming before irreversible tissue remodelling occurs. - Source: PubMed
Publication date: 2026/09/10
Kuchay Mohammad ShafiCubero Francisco JavierRamos-Molina Bruno - Genetic variants involved in lipid and glucose metabolism have been implicated in liver disease progression and hepatocellular carcinoma (HCC) development in patients with metabolic dysfunction-associated steatotic liver disease (MASLD). However, their prognostic role in patients with established HCC remains unclear. We aimed to investigate the association between MASLD-related genetic variants and overall survival (OS) in patients with MASLD-related HCC. - Source: PubMed
Publication date: 2026/08/12
Guariglia MartaCaviglia Gian PaoloGaia SilviaRosso ChiaraRolle EmanuelaSaba FrancescaDileo EleonoraSilvestri Gemma MartinaArmandi AngeloCarucci PatriziaBugianesi Elisabetta - Metabolic dysfunction-associated steatotic liver disease (MASLD) has traditionally been conceptualized as a predominantly metabolic disorder driven by obesity and insulin resistance. However, recent advances in human genetics have revealed a more complex picture that encompasses germline susceptibility variants, protective loss-of-function alleles, polygenic risk models, and somatic clonal evolution. Since the discovery of PNPLA3 (patatin-like phospholipase domain-containing 3) I148M, multiple loci-including TM6SF2, MBOAT7, GCKR, HSD17B13, MTARC1, GPAM, and CIDEB-have substantially expanded the mechanistic understanding of disease heterogeneity and hepatocellular vulnerability. Recent studies integrating partitioned polygenic risk scores and unsupervised phenotypic clustering suggest that MASLD may be organized into at least two predominant subtypes: a liver-specific subtype characterized by intrinsic hepatocellular susceptibility, and a cardiometabolic subtype associated with systemic metabolic dysfunction and increased cardiovascular risk. Analyses of cirrhotic liver tissue have, in turn, demonstrated somatic clonal expansion of hepatocytes harboring adaptive metabolic mutations, adding an evolutionary dimension to advanced disease. On this basis, we propose an integrated LS/CM/C framework encompassing liver-specific (LS), cardiometabolic (CM), and clonal (C) components. This model offers a conceptual structure that links germline genetics, metabolic heterogeneity, somatic adaptation, and emerging pharmacogenomic strategies. The recent development of genotype-directed therapies targeting PNPLA3 and HSD17B13, together with the approval of resmetirom and semaglutide, further supports the transition toward biologically stratified hepatology. Although prospective validation remains necessary, the convergence of genetics, clonal biology, and targeted therapeutics suggests that MASLD is moving toward an era of precision medicine. - Source: PubMed
Publication date: 2026/07/24
Crespo JavierAlonso-Peña MartaJiménez-González CarolinaCayón-Gonzalez LorenaIruzubieta Paula